title: Preconditioning with triiodothyronine improves the clinical signs and acute tubular necrosis induced by ischemia/reperfusion in rats.
abstract: BACKGROUND
  Renal ischemia/reperfusion (I/R) injury is manifested by acute renal failure (ARF) and acute tubular necrosis (ATN). The aim of this study was to evaluate the effectiveness of preconditioning with 3, 3, 5 triiodothyronine (T3) to prevent I/R renal injury.
  
  
  RESULTS
  The rats were divided into four groups: sham-operated, placebo-treated (SO-P), sham-operated T3- treated (SO- T3), I/R-injured placebo-treated (IR-P), and I/R-injured T3-treated (IR- T3) groups. At 24 h before ischemia, the animals received a single dose of T3 (100 μg/kg). Renal function and plasma, urinary, and tissue variables were studied at 4, 24, and 48 h of reperfusion, including biochemical, oxidative stress, and inflammation variables, PARP-1 immunohistochemical expression, and ATN morphology. In comparison to the SO groups, the IR-P groups had higher plasma urea and creatinine levels and greater proteinuria (at all reperfusion times) and also showed: increased oxidative stress-related plasma, urinary, and tissue variables; higher plasma levels of IL6 (proinflammatory cytokine); increased glomerular and tubular nuclear PARP-1 expression; and a greater degree of ATN. The IR-T3 group showed a marked reduction in all of these variables, especially at 48 h of reperfusion. No significant differences were observed between SO-P and SO-T3 groups.
  
  
  CONCLUSIONS
  This study demonstrates that preconditioning rats with a single dose of T3 improves the clinical signs and ATN of renal I/R injury. These beneficial effects are accompanied by reductions in oxidative stress, inflammation, and renal PARP-1 expression, indicating that this sequence of factors plays an important role in the ATN induced by I/R injury.
authors.affiliation: Servicio de Nefrología, Unidad Experimental, Hospital Virgen de las Nieves, Granada, Spain.
authors.forename: Carla
authors.initials: C
authors.lastname: Ferreyra
authors.forename: Félix
authors.initials: F
authors.lastname: Vargas
authors.forename: Isabel
authors.initials: I
authors.lastname: Rodríguez-Gómez
authors.forename: Rocío
authors.initials: R
authors.lastname: Pérez-Abud
authors.forename: Francisco
authors.initials: F
authors.lastname: O'Valle
authors.forename: Antonio
authors.initials: A
authors.lastname: Osuna
mesh_terms: D000818:Animals; D001706:Biopsy; D005978:Glutathione / Q000097:blood; D007150:Immunohistochemistry; D007249:Inflammation / Q000150:complications / Q000473:pathology; D015850:Interleukin-6 / Q000097:blood; D019194:Ischemic Preconditioning; D007668:Kidney / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D007677:Kidney Function Tests; D007683:Kidney Tubular Necrosis, Acute / Q000097:blood / Q000209:etiology* / Q000503:physiopathology / Q000652:urine; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000097:blood / Q000150:complications* / Q000503:physiopathology / Q000652:urine; D014284:Triiodothyronine / Q000494:pharmacology*
chemical_list: D015850:Interleukin-6; D014284:Triiodothyronine; D008315:Malondialdehyde; D005978:Glutathione